Viral respiratory infections are frequent precipitants in an attack of asthma. The role virus may play in impairing the beta-adrenergic response is being investigated. Granulocytes will secrete lysosomal enzymes when incubated with complement coated zymosan particles. Isoproterenol inhibits this response. During viral respiratory infections precipitating asthma, this beta-adrenergic response is impaired. A similar reduction in isoproterenol activity occurs when isolated human granulocytes are incubated with rhinovirus 16. We propose to study the mechanism by which this occurs and specifically to quantitate the number and affinity of beta-adrenergic receptors with the radioligands 125I-hydroxybenzyl-pindolol. In addition we have found that parainfluenza 3 infected ovalbumin guinea pigs may provide an animal model for asthma. In these virus infected animals there is selective blockade of the beta-adrenergic mediated inhibition of antigen-induced contraction of airway smooth muscle and, presumably, mediator release. The currnet proposal will examine whether changes in the beta receptor can explain the inhibitory effects of virus infection.